Fetal cerebral Doppler in the recognition of fetal compromise.

OBJECTIVE: To establish reference ranges for the human fetal middle cerebral artery pulsatility index (MCA PI) for the local obstetric population, and to compare computerised antenatal fetal heart rate (FHR) analysis with the MCA PI as indicators of fetal compromise. DESIGN: Prospective data collection for selected patients. SETTING: High risk pregnancy unit of a teaching hospital. SUBJECTS: Group 1 consisted of 18 healthy women with uncomplicated singleton pregnancies. Group 2 consisted of 27 women admitted to the high risk pregnancy unit over a 9 month period with intrauterine growth retardation and other related problems; all these women were delivered by prelabour caesarean section. INTERVENTION: Serial Duplex sonography to determine fetal MCA PI in Groups 1 and 2. Serial FHR analysis using computerised numerical techniques in Group 2 only. MAIN OUTCOME MEASURES: Serial MCA PI values from 24 to 39 completed weeks of gestation in Group 1. Comparison of serial MCA PI values with FHR analysis in relation to fetal outcome in Group 2. RESULTS: In Group 1 the MCA PI diminished significantly as gestation advanced from 1.73 (SD 0.25) at 24 weeks to 1.38 (SD 0.26) at 39 weeks (P < 0.01). In Group 2 eleven babies were hypoxaemic at delivery: all had low MCA PI values while only nine had an abnormal FHR prior to delivery. CONCLUSION: In normal pregnancy, there is a fall in the fetal MCA PI with advancing gestation which probably reflects a decreasing vascular resistance to fetal cerebral blood flow. Hypoxaemia at delivery appeared to be better recognised by the fetal MCA flow velocity waveform than the FHR analysis. This increased sensitivity, however, was achieved at the expense of a reduced specificity. Larger studies are needed to confirm the findings of this preliminary investigation.

The influence of spontaneous and induced labour on the rise in prostaglandins at amniotomy.

Maternal peripheral plasma levels of 13,14-dihydro-15-keto-prostaglandin F (PGFM) were measured immediately before and 5 min after amniotomy. Three groups of women were studied: women in late pregnancy; women in spontaneous labour; and women who had received intravaginal prostaglandin E2 (PGE2) pessary. There was no significant difference in the magnitude of the rise in PGFM after amniotomy in late pregnancy or during spontaneous labour suggesting that labour has no influence on the release of prostaglandin F2 alpha (PGF2 alpha) induced by artificial rupture of the fetal membranes. However, local administration of PGE2 before amniotomy caused a greater rise in PGFM suggesting that PGE2 can influence the release and/or metabolism of PGF2 alpha.

Raised prostaglandin levels in the third stage of labor.

Serial measurements of maternal peripheral plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F (PGFM) and oxytocin were made during the three stages of labor and in the immediate puerperium. PGFM levels increased a labor progressed, and reached maximal levels before placental separation had occurred. The mean value in the second stage of labor was significantly higher than that in the first stage (p less than 0.01); similarly, the value 5 minutes after delivery, before expulsion of the placenta, was significantly greater than that in the second stage of labor (p less than 0.01). There was no significant difference between the mean PGFM concentration at placental separation and the level 5 minutes after delivery or in the second stage of labor. Two hours after delivery of the placenta, PGFM levels were not significantly different from values observed in the first stage of labor. Peripheral plasma concentrations of oxytocin did not change significantly at any stage of labor or 2 hours post partum. These results suggest that prostaglandins have a role in the third stage of labor, and this finding may have important clinical implications.

The relation between the release of prostaglandins at amniotomy and the subsequent onset of labour.

Maternal peripheral plasma levels of 13,14-dihydro-15-keto-prostaglandin F (PGFM) were measured in 16 women following amniotomy performed for the induction of labour at term. After 5 1/2 hours, seven patients were in established labour (Group I) but the remaining nine patients required an intravenous infusion of oxytocin (Group II). An initial rapid rise in PGFM concentrations within five minutes of amniotomy occurred in all women and, therefore, the onset of labour does not appear to be a direct consequence of this initial increase. In Group I there was a significant increase in PGFM concentrations between five and 30 minutes after amniotomy and from 30 minutes to the time at which the last sample was collected; these later rises were associated with the onset and progress of labour in these women. These increases in PGFM concentrations did not occur in patients in Group II. The reason for this difference in response to amniotomy is as yet unclear.

Is oxytocin involved in parturition?

Peripheral plasma levels of oxytocin were determined in women during pregnancy and labour. There was a significant increase in maternal plasma oxytocin with advancing gestation but no significant change in levels at any stage of labour. Oxytocin concentrations in umbilical cord plasma were measured after spontaneous vaginal delivery and at elective caesarean section. A significant arteriovenous difference, with higher arterial levels, was found in both groups and the values after labour were significantly higher tha at elective caesarean section. These findings suggest that the fetus is able to produce oxytocin which may play a role in human parturition.

A comparison of plasma prostaglandin levels in term and preterm labour.

Peripheral plasma levels of 13,14-dihydro-15-keto-prostaglandin F (PGFM) were determined in women during pregnancy and in term and preterm labour. The PGFM concentrations at term were not significantly different from the levels between 26 and 34 weeks gestation. In both term and preterm labour there was a rise in PGFM levels with increasing cervical dilatation although the mean values tended to be lower during preterm labour. These findings may provide an explanation for the effectiveness of prostaglandin synthetase inhibitors in suppressing myometrial activity in preterm labour.

Release of prostaglandins after amniotomy is not mediated by oxytocin.

The rise in peripheral plasma levels of 13,14-dihydro-15-keto-prostaglandin F (PGFM) following amniotomy has now been shown to be maximal within five minutes of the procedure, and levels remain elevated for at least 30 minutes. There was no change in plasma oxytocin levels with amniotomy and therefore a local mechanism for prostaglandin release has been postulated.

In vivo antiviral properties of biologically active compounds. II. Studies with influenza and vaccinia viruses.

The in vivo anti-influenza virus and antivaccinia virus activity of 156 biologically active compounds was determined. One of two criteria was used for evaluating activity against the influenza virus. The criteria were increase in survivor number and mean survival time, and reduction in virus-induced lung consolidation in treated, infected Swiss mice. Increase in survivor number and mean survival time were the criteria for evaluation of antivaccinia virus activity. Several drug doses were tested against two virus concentrations to demonstrate antiviral activity more clearly. Two compounds were considered significantly active against the influenza virus: DL-noformicin (NSC 72942) and amantadine hydrochloride (NSC 83653). Eleven compounds had reproducible activity against vaccinia virus: isatin-beta-thiosemicarbazone (NSC 721), 6-azauracil (NSC 3425), 9-alpha-fluoro-2alpha-methylhydrocortisone 21-acetate (NSC 12601), 5-[bis(2-chloroethyl)amino]uracil (NSC 34462), 5-iodo-2'-deoxyuridine (NSC 39661), streptonigrin (NSC 45383), N-methylisatin beta-thiosemicarbazone (NSC 69811), cytovirin (NSC 91770), 9-beta-D-arabinofuranosyladenine (NSC 404241), and 5-(mercaptomethyl)uracil (NSC 529351).